1. Sera of 92 epileptic patients, receiving phenytoin (3-7mg/kg/per day) alone/ in combination with phenobarbitone (1-2 mg/kg/day), were analysed for total and free phenytoin spectrophotometrically.
2. The respective means of total and free phenytoin in the phenytoin group were not significantly different from the phenytoin plus phenobarbitone group.
3. The relationshp between total and free phenytoin, in all patients, was curvilinear i.e. biphasic. The proportion of free phenytoin in patients with total phenytoin <20(g/ml was significantly (p<0.01) higher than those with total phenytoin <20 (g/ml
4. Compared to uncontrolled patients the controlled patients without toxicity showed no statistical differences in mean levels of total and free phenytoin; significantly higher proportion of free drug and a tendency to maintain higher levels of both free and total drug at a given dose, and a significant rise in these levels with dosage increment.
5. The mean total and free phenytoin levels in patients who developed toxicity were higher than the uncontrolled as well as controlled patients without toxicity.

1. Interaction of tolbutamide with some betaadrenoceptor antagonist was studied in normal and alloxan-induced diabetic rabbits.
2. Propranolol and atenolol per se produced hypoglycaemia and potentiated tolbutamide effect also. However, on concurrent administration they failed to influence serum concentration pattern and half life of tolbutamide in normal as well as diabetic rabbits.
3. Metoproiol and acebutolol, both cardio-selective ( blockers, per se neither produced any change in blood sugar level nor influenced tolbutamide hypoglycaemia and its serum level.
4. In diabetic rabbits, all the (adrenergic blockers studied, potentiated tolbutamide hypoglycaemia.
5. In the animals pretreated with (adrenergic blockers for 7days,only propranolol and atenoiol potentiated tolbutamide hypoglycaemia but the serum tolbutamide level remained unchanged.

1. Adenine nucleotides produced contraction dependent contraction of crop. The order of potency was: ATP> ADP> AMP. The response of ATP was blocked by promethazine, cyproheptadine, caffeine and partially reduced by atropine. Electrical stimulation of the innervating nerves caused a contraction followed by relaxation up to 80 percent.
2. Electrical Stiulation of the innervating nerves caused a constraction followed by relaxation up to 80 percent.
3. The initial contraction was blocked by atropine and the residual contraction was blocked by cyproheptadine. The response was almost completely blocked by promethazine (104 M) but was not altered at all by caffeine (10 M) tolazoline (104 M) or propranolol (104 M)
4. lt is likely that ATP is acting on the release or receptors of histamine or 5-HT.

1. In the present study it has been shown that acetylsalicylic acid (ASA) produces hemolysis of both normal and G-6-PD deficient erythrocytes.
2. The degree of hemolysis is almost the same in both the erythrocytes.
3. Acetylation and peroxidation of membrane lipid do not appear to be necessary for the hemolytic effect of ASA.
4. Severe membrane damage as evident from the liberation of phospholipids and sterols appears to be the mechanism by which ASA produces hemolysis.

1. The study was conducted in 5 healthy human volunteers to compare the effect on heart rate and blood pressure of three (2 , stimulants, salbutamol (4 mg) terbutaline (5 mg) and orciprenaline (20 mg). Two beta blockers, propranolol (40 mg) and metoprolol (50 mg) were also used to elucidate underlying mechanisms
2. All three (2 stimulants produced increase in heart rate (HR) and systolic BP and a fall in diastolic BP.
3. Effect on HR seems to be through cardiac (land. (2 receptors.
4. Effect on syst. B P seems to be through (I receptors.
5. Fall in diastolic B P seems to be mediated through (2 receptors.